Association of mannose binding lectin codon 54 polymorphism with predisposition to Henoch-Schönlein purpura in childhood

PubMed ID: 24576294Aim: Immune and inflammatory response activation is a common feature of systemic vasculitis. There is a protein called mannose binding lectin (MBL) that was reported to play an important role in innate immunity. MBL polymorphisms in the MBL gene cause predisposition to infectious and autoimmune diseases. There is no study in the literature investigating the association between MBL polymorphisms and Henoch-Schönlein purpura (HSP) to date. Therefore, the aim of this study is to determine the presence of any association between MBL gene variants and HSP in a child population. Method: Codon 54 polymorphism in exon 1 of the MBL gene was investigated by polymerase chain reaction - restriction fragment length polymorphism method in 100 children diagnosed as having HSP and 100 age-matched healthy controls. Results: The mutant B allele frequency was not significantly higher in the patient group (16%) compared to the control group (14%). AB genotype was found to be 28% and 26% in the patient group and healthy control group, respectively. AA genotype was found in 70% of the children with HSP and 73% of the healthy control group. Conclusion: These results suggest that codon 54 polymorphism in the MBL gene may hardly play a role in susceptibility to HSP in children, the first time this has been reported in the literature. © 2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd

Effect of vildagliptin add-on treatment to metformin on plasma asymmetric dimethylarginine in type 2 diabetes mellitus patients

Mustafa Cakirca,1 Cumali Karatoprak,1 Mehmet Zorlu,1 Muharrem Kiskac,1 Mustafa Kanat,2 Mehmet Ali Cikrikcioglu,1 Pinar Soysal,3 Mehmet Hursitoglu,4 Ahmet Adil Camli,1 Reha Erkoc,1 Muhammad Abdul-Ghani5 1Internal Medicine Clinic, Faculty of Medicine, Bezmialem Vakif University, 2Department of Internal Medicine, Medical Faculty, Istanbul Medipol University, 3Department of Geriatric Medicine, Medical Faculty, Dokuz Eylül University, 4Department of Internal Medicine, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul, Turkey; 5Division of Medicine – Diabetes, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Aims: A close association has been demonstrated between increased cardiovascular risk and high asymmetric dimethylarginine (ADMA) levels in type 2 diabetes mellitus (DM) patients. We planned to measure serum ADMA levels in type 2 DM patients using vildagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor. Materials and methods: A total of 68 type 2 DM patients who were on metformin were enrolled in the study. Based on the glycemic levels of patients, vildagliptin was added on to treatment in 33 patients. Patients were followed for 6 months. Serum ADMA, C-reactive protein, and fibrinogen levels were compared in groups of patients using metformin or metformin + vildagliptin, after 6 months. Results: Serum ADMA levels were found to be significantly lower in the group using vildagliptin compared to the group using metformin + vildagliptin (P<0.001). However, serum C-reactive protein and fibrinogen levels were statistically similar in the two study groups (P=0.34 and P=0.23, respectively). Conclusion: Metformin + vildagliptin treatment was observed to lower serum ADMA levels in type 2 DM patients. Our findings notwithstanding, large-scale prospective randomized controlled studies are warranted to conclude that vildagliptin provides cardiovascular protection along with diabetes regulation. Keywords: asymmetric dimethylarginine (ADMA), dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, type 2 diabetes mellitu